Premium
Exercise Paradoxically Modulates Bioactivities of Tissue Factor and Matrix Metalloproteinase Induced by Platelets Interaction with Nasopharyngeal Carcinoma Cells
Author(s) -
Wang Jong Shyan,
Chang Chun Ying,
Chou Wan Yu
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a931-a
Subject(s) - tissue factor pathway inhibitor , platelet , tissue factor , coagulation , fibrinogen , nasopharyngeal carcinoma , medicine , chemistry , platelet activation , tissue inhibitor of metalloproteinase , endocrinology , matrix metalloproteinase , metalloproteinase , immunology , radiation therapy
This investigation explores how different exercise regimens affect heterotypic aggregation, as well as expressions/activities of tissue factor (TF)/tissue factor pathway inhibitor (TFPI) and matrix metalloproteinase (MMP)‐2 and ‐9/tissue inhibitor of metalloproteinase‐1 (TIMP‐1) induced by platelet‐nasopharyngeal carcinoma cell (NPC) interactions. Thirty sedentary men performed on three occasions moderate‐intensity exercise (MIE, 60% VO 2max for 40 min) and high‐intensity exercise (HIE, up to VO 2max ) with and without warm‐up exercise (WUE, 60% VO 2max for 20 min) on a bicycle ergometer. The results of this study demonstrated that HIE enhanced platelet‐NPC aggregation and platelet‐promoted TF activity/expression of NPC in the presence of fibrinogen, and was accompanied by an increase in TIMP‐1 level and decreases in MMP‐2 and ‐9 activities and TFPI content under conditions of platelet‐NPC co‐incubation, whereas these alterations to HIE on platelet‐NPC interactions were ameliorated by WUE pretreatment. Conversely, MIE lowered the formation of platelet‐NPC aggregates induced by fibrinogen, but did not change TF, TFPI, MMP‐2 and ‐9, and TIMP‐1 activities or/and expressions induced by platelet‐NPC interactions. We conclude that HIE enhances aggregation and coagulation, and reduce matrix degradation related with platelet‐NPC interactions, by raising the binding affinity to fibrinogen, TF expression/activity and TMIP release, and lowering TFPI release and MMP‐2/‐9 activities. These effects on HIE diminish after WUE. However, MIE minimizes the risk of thrombosis induced by platelet‐NPC interactions.